Woodman J P, Dimier I H, Bout D T
Unité de Recherche Université-INRA d'Immunologie Parasitaire, UFR des Sciences Pharmaceutiques de Tours, France.
J Immunol. 1991 Sep 15;147(6):2019-23.
Toxoplasma gondii invaded and proliferated in cultured human umbilical vein endothelial cells. Preincubation of the human umbilical vein endothelial cells with human rIFN-gamma induced a high degree of inhibition of T. gondii replication, with the effect being dose dependent. In order to try to elucidate the inhibitory mechanism, we tested the presence of several factors that are known to operate against intracellular parasites in other cell types. We found, by means of a competitive inhibitor, that L-arginine-dependent production of reactive nitrogen intermediates was not the cause of inhibition of T. gondii proliferation, thus contrasting with the inhibitory mechanism found in activated mouse macrophages. Furthermore, the inhibition of replication was not overcome by oxygen scavengers or by saturation of the system with tryptophan, suggesting that neither reactive oxygen intermediates nor the induction of tryptophan starvation was responsible.
刚地弓形虫侵入培养的人脐静脉内皮细胞并在其中增殖。用人重组干扰素-γ预孵育人脐静脉内皮细胞可高度抑制刚地弓形虫的复制，且该效应呈剂量依赖性。为了阐明抑制机制，我们检测了几种已知在其他细胞类型中作用于细胞内寄生虫的因子的存在情况。我们通过一种竞争性抑制剂发现，依赖L-精氨酸产生的活性氮中间体不是抑制刚地弓形虫增殖的原因，这与在活化的小鼠巨噬细胞中发现的抑制机制形成对比。此外，氧清除剂或用色氨酸使系统饱和并不能克服复制的抑制，这表明活性氧中间体和色氨酸饥饿的诱导均不是其原因。
